Retinal photoreceptors of albino rats, when exposed to intense, cyclic incandescent, or low intensity, continuous fluorescent illumination gradually undergo severe damage and are destroyed and removed from the eye. Prior to puberty, the photoreceptors are more resistent to photic damage than after adulthood. Concurrent with the onset of pubertal changes, the damage progressively becomes more severe. After ovariectomy of young and adult rats, photoreceptors are more resistent to photic damage than after sham-operation. Hypophysectomy is equally effective. The objectives of the proposed project are to examine the influence of the pituitary gland and its target organs, through their hormones, on photically-induced and hereditary retinopathies. Synergistic relations between gonadal and pituitary hormones, such as testosterone, estrogen and prolactin will be related to the development of retinal damage. In addition to prolactin, other hormones, such as those of the adrenal gland and insulin, will be included in the project. Light and electron microscopic evaluations of the structural changes will be quantified and compared to serum hormonal levels in control and experimental groups. The origin, migratory pattern and distribution of intraretinal macrophages will be recorded using autoradiographic techniques in albino, pigmented, and RCS rats with hereditary retinal dystrophy. Retinal changes in streptozotocin-induced diabetic rats, exposed to cyclic light and to light intensities which damage the retina, will be correlated with the hormonal status of the animals. The mechanism by which stress affects hereditary retinal dystrophy and light-induced damage will be examined. Pharmacologic agents which regulate dopamine metabolism in the CNS and consequently, the secretion of prolactin, will be injected and evaluated for their enhancement or amelioration of retinal photoreceptor damage.